Chapter 13. Memory, Learning, and Development

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Ingfei Chen In a white lab coat and blue latex gloves, Neda Vishlaghi peers through a light microscope at six milky-white blobs. Each is about the size of a couscous grain, bathed in the pale orange broth of a petri dish. With tweezers in one hand and surgical scissors in the other, she deftly snips one tiny clump in half. When growing human brains, sometimes you need to do some pruning. The blobs are 8-week-old bits of brainlike tissue. While they wouldn’t be mistaken for Lilliputian-sized brains, some of their fine-grained features bear a remarkable resemblance to the human cerebral cortex, home to our memories, decision making and other high-level cognitive powers. Vishlaghi created these “minibrains” at the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA, where she’s a research assistant. First she immersed batches of human pluripotent stem cells — which can morph into any cell type in the body — in a special mix of chemicals. The free-floating cells multiplied and coalesced into itty-bitty balls of neural tissue. Nurtured with meticulously timed doses of growth-supporting ingredients, the cell clumps were eventually transferred to petri dishes of broth laced with Matrigel, a gelatin-like matrix of proteins. On day 56, the blobs display shadowy clusters of neural “rosettes.” Under a laser scanning microscope, razor-thin slices of those rosettes reveal loose-knit layers of a variety of dividing neural stem cells and the nerve cells, or neurons, they give rise to. The layered structures look similar to the architecture of a human fetal brain at 14 weeks of gestation. |© Society for Science & the Public 2000 - 2018

Keyword: Development of the Brain
Link ID: 24686 - Posted: 02.21.2018

Sarah Webb Four years ago, scientists from Google showed up on neuroscientist Steve Finkbeiner’s doorstep. The researchers were based at Google Accelerated Science, a research division in Mountain View, California, that aims to use Google technologies to speed scientific discovery. They were interested in applying ‘deep-learning’ approaches to the mountains of imaging data generated by Finkbeiner’s team at the Gladstone Institute of Neurological Disease in San Francisco, also in California. Deep-learning algorithms take raw features from an extremely large, annotated data set, such as a collection of images or genomes, and use them to create a predictive tool based on patterns buried inside. Once trained, the algorithms can apply that training to analyse other data, sometimes from wildly different sources. The technique can be used to “tackle really hard, tough, complicated problems, and be able to see structure in data — amounts of data that are just too big and too complex for the human brain to comprehend”, Finkbeiner says. He and his team produce reams of data using a high-throughput imaging strategy known as robotic microscopy, which they had developed for studying brain cells. But the team couldn’t analyse its data at the speed it acquired them, so Finkbeiner welcomed the opportunity to collaborate. “I can’t honestly say at the time that I had a clear grasp of what questions might be addressed with deep learning, but I knew that we were generating data at about twice to three times the rate we could analyse it,” he says. © 2018 Macmillan Publishers Limited,

Keyword: Learning & Memory; Robotics
Link ID: 24684 - Posted: 02.21.2018

By GRETCHEN REYNOLDS Exercise may help the brain to build durable memories, through good times and bad. Stress and adversity weaken the brain’s ability to learn and retain information, earlier research has found. But according to a remarkable new neurological study in mice, regular exercise can counteract those effects by bolstering communication between brain cells. Memory has long been considered a biological enigma, a medley of mental ephemera that has some basis in material existence. Memories are coded into brain cells in the hippocampus, the brain’s memory center. If our memories were not written into those cells, they would not be available for later, long-term recall, and every brain would be like that of Dory, the memory-challenged fish in “Finding Nemo.” But representations of experience are extremely complex, and aspects of most memories must be spread across multiple brain cells, neuroscientists have determined. These cells must be able to connect with one another, so that the memory, as a whole, stays intact. The connections between neurons, known as synapses, are composed of electrical and chemical signals that move from cell to cell, like notes passed in class. The signals can be relatively weak and sporadic or flow with vigor and frequency. In general, the stronger the messages between neurons, the sturdier and more permanent the memories they hold. Neuroscientists have known for some time that the potency of our synapses depends to some degree on how we live our lives. Lack of sleep, alcohol, diet and other aspects of our lifestyles, especially stress, may dampen the flow of messages between brain cells, while practice fortifies it. Repeat an action and the signals between the cells maintaining the memory of that action can strengthen. That is learning. © 2018 The New York Times Company

Keyword: Learning & Memory
Link ID: 24683 - Posted: 02.21.2018

Heavy drinkers are putting themselves at risk of dementia, according to the largest study of its kind ever conducted. Research published in the Lancet Public Health journal provides powerful evidence that people who drink enough to end up in hospital are putting themselves at serious risk of vascular dementia and Alzheimer’s disease. It will also raise questions for moderate drinkers about the possible long-term consequences of their social habit. The study, which used the French National Hospital Discharge database, looked at more than a million people diagnosed with dementia between 2008 and 2013. More than a third – 38% of the 57,000 cases of early-onset dementia – were directly alcohol-related and 18% had an additional diagnosis of alcohol use disorders. Overall, alcohol use disorders were associated with a three times greater risk of all types of dementia. Dr Sara Imarisio, head of research at Alzheimer’s Research UK, said: “As this study only looked at the people who had been admitted to hospital due to chronic heavy drinking, it doesn’t reveal the full extent of the link between alcohol use and dementia risk. Previous research has indicated that even moderate drinking may have a negative impact on brain health and people shouldn’t be under the impression that only drinking to the point of hospitalisation carries a risk.” Experts said the new research should change attitudes. “What is most surprising about this paper is that it has taken us so long to recognise that alcohol misuse and dependence are such potent risk factors for the development of dementia,” said Robert Howard, professor of old age psychiatry at University College London.

Keyword: Drug Abuse; Alzheimers
Link ID: 24682 - Posted: 02.21.2018

Jon Hamilton Beer has fueled a lot of bad ideas. But on a Friday afternoon in 2007, it helped two Alzheimer's researchers come up with a really a good one. Neuroscientists Robert Moir and Rudolph Tanzi were sipping Coronas in separate offices during "attitude adjustment hour" at Massachusetts General Hospital, Harvard's largest teaching hospital. And, by chance, each scientist found himself wondering about an apparent link between Alzheimer's disease and the immune system. Moir had been surfing through random scientific papers online — something he does for an hour or so on most Fridays. "I cruise wherever my fancy takes me," he says. And on this day, he cruised to research on molecules known as antimicrobial peptides. They're part of the ancient immune system that's found in all forms of life and plays an important role in protecting the human brain. One way antimicrobial peptides protect us is by engulfing and neutralizing a germ or some other foreign invader. That gives newer parts of the immune system time to get mobilized. These peptides are "extremely important," Moir says. "They're not like legacies from an immune system we don't use anymore. If you don't have them, you're going to die in a couple of hours." As Moir surfed through paper after paper, he realized that one of these ancient molecules, known as LL-37, looked a lot like a molecule closely associated with Alzheimer's. That molecule is called amyloid-beta and it forms the sticky plaques that tend to build up in the brains of people with dementia. © 2018 npr

Keyword: Alzheimers; Neuroimmunology
Link ID: 24680 - Posted: 02.19.2018

Laurel Hamers AUSTIN, Texas — Babies’ stroke-damaged brains can pull a mirror trick to recover. A stroke on the left side of the brain often damages important language-processing areas. But people who have this stroke just before or after birth recover their language abilities in the mirror image spot on the right side, a study of teens and young adults shows. Those patients all had normal language skills, even though as much as half of their brain had withered away, researchers reported February 17 at the annual meeting of the American Association for the Advancement of Science. Researchers so far have recruited 12 people ages 12 to 25 who had each experienced a stroke to the same region of their brain’s left hemisphere just before or after birth. People who have this type of stroke as adults often lose their ability to use and understand language, said study coauthor Elissa Newport, a neurology researcher at Georgetown University Medical Center in Washington, D.C. MRI scans of healthy siblings of the stroke patients showed activity in language centers in the left hemisphere of the brain when the participants heard speech. The stroke patients showed activity in the exact same areas — just on the opposite side of the brain. It’s well established that if an area of the brain gets damaged, other brain areas will sometimes compensate. But the new finding suggests that while young brains have an extraordinary capacity to recover, there might be limits on which areas can pinch-hit. |© Society for Science & the Public 2000 - 2018.

Keyword: Laterality; Stroke
Link ID: 24678 - Posted: 02.19.2018

By John Carroll, For years now the gold standard for R&D in Alzheimer’s disease has focused on generating convincing evidence that any new therapy being studied could slow the cognitive decline of patients and help preserve their ability to perform the kind of daily functions that can keep a patient independent for a longer period of time. That’s a hurdle no one has managed to clear for well over a decade. So now, with late-stage clinical failures piling up, the U.S. Food and Drug Administration (FDA) has set off down a path to adapt those standards as researchers are pushed inexorably into earlier and earlier forms of the disease, ahead of the brain damage inflicted by Alzheimer’s. In a set of draft guidances, the agency essentially proposed to offer an approval pathway for new drugs that could prevent the onset of the devastating symptoms of Alzheimer’s if drug developers could hit acceptable biomarkers that indicate the drug is working. And they’re likely going to continue with a new gold standard that will focus on long-term cognition alone, lowering the bar for drugs for an enormous and growing market. David Miller, the clinical vice president of Bracket, a Washington, D.C.-based tech provider which specializes in Alzheimer’s studies, tells me the draft guidance hit just after a meeting of the Washington, D.C.-based Alzheimer’s Association research group, which was discussing how you might be able to use a mix of markers for amyloid β and tau—two toxic proteins frequently cited as likely triggers—alongside neurodegenerative markers to identify patients who could be enrolled at a very early point in the disease. © 2018 American Association for the Advancement of Science.

Keyword: Alzheimers
Link ID: 24674 - Posted: 02.17.2018

Nicola Davis Pilot studies have shown that changes in vesicles in men’s semen mirror that in their sperm, suggesting that, as in mice, the two interact. Pilot studies have shown that changes in vesicles in men’s semen mirror that in their sperm, suggesting that, as in mice, the two interact. Photograph: Alamy Stressed fathers may end up with changes to their sperm that could affect behaviour in their offspring, research in mice has shown. Previous work by the team found that male mice who were exposed to a mildly stressful event, such as being restrained, produced sperm that was richer in certain types of molecules called microRNAs. Crucially, the higher levels of these microRNAs in the sperm seemed to result in offspring with a dampened response to stress. That, scientists have noted, could affect the mental health of offspring, since an inability to respond appropriately to stress has been linked to neuropsychiatric disorders such as PTSD and depression. “The hypothalamus, the part of the brain that determines your stress response, has been wired differently,” said Tracy Bale, professor of neuroscience at the University of Maryland School of Medicine, who is presenting the new research at the meeting of the American Association for the Advancement of Science in Austin, Texas. Now the researchers say they have unpicked what is going on through work in both mice and cultured cells – experiments known as “stress in the dish”.

Keyword: Stress; Epigenetics
Link ID: 24673 - Posted: 02.17.2018

By Roni Dengler AUSTIN—Babies are as primed to learn a visual language as they are a spoken one. That’s the conclusion of research presented here today at the annual meeting of AAAS, which publishes Science. Parents and scientists know babies are learning sponges that can pick up any language they’re born into. But not as much is known about whether that includes visual language. To find out if infants are sensitive to visual language, Rain Bosworth, a psychologist at the University of California, San Diego, tracked 6-month-olds’ and 1-year-olds’ eye movements as they watched a video of a woman performing self-grooming gestures, such as tucking her hair behind her ear, and signing. The infants watched the signs 20% more than the 1-year-old children did. That means babies can distinguish between what’s language and what’s not, even when it’s not spoken, but 1-year-olds can’t. That’s consistent with what researchers know about how babies learn spoken language. Six-month-olds home in on their native language and lose sensitivity to languages they’re not exposed to, but by 12 months old that’s more or less gone, Bosworth says. The researchers also watched babies’ gazes as they observed a signer “fingerspelling,” spelling out words with individually signed letters. The signer executed the fingerspelling cleanly or sloppily. Again, researchers found the 6-month-old babies, who had never seen sign language before, favored the well-formed letters, whereas the 12-month-olds did not show a preference. Together that means there’s a critical developmental window for picking up even nonverbal languages. As 95% of deaf children are born to hearing parents, they are at risk for developmental delays because they need that language exposure early on, the scientists say. © 2018 American Association for the Advancement of Science

Keyword: Language; Development of the Brain
Link ID: 24672 - Posted: 02.17.2018

A small group of cells in the brain can have a big effect on seizures and memory in a mouse model of epilepsy. According to a new study in Science, loss of mossy cells may contribute to convulsive seizures in temporal lobe epilepsy (TLE) as well as memory problems often experienced by people with the disease. The study was funded by the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health. “The role of mossy cells in epilepsy has been debated for decades. This study reveals how critical these cells are in the disease, and the findings suggest that preventing loss of mossy cells or finding ways to activate them may be potential therapeutic targets,” said Vicky Whittemore, Ph.D., program director at NINDS. Mossy cells, named for the dense moss-like protrusions that cover their surface, are located in the hippocampus, a brain area that is known to play key roles in memory. Loss of mossy cells is associated with TLE, but it is unknown what role that plays in the disease. Using state-of-the-art tools, Ivan Soltesz, Ph.D., professor of neurosurgery and neurosciences at Stanford University, Palo Alto, California, and his team were able to turn mossy cells on and off to track their effects in a mouse model of epilepsy. “This study would not have been possible without the rapid advancement of technology, thanks in part to the BRAIN Initiative, which has encouraged scientists to develop innovative instruments and new ways to look at the brain,” said Dr. Soltesz. “It’s remarkable that we can manipulate specific brain cells in the hippocampus of a mouse. Using 21st century tools brings us closer than ever to unlocking the mysteries behind this debilitating disease.”

Keyword: Epilepsy; Learning & Memory
Link ID: 24669 - Posted: 02.16.2018

By Ashley Yeager Wandering through a maze with striped gray walls, a mouse searches for turns that will take it to a thirst-quenching reward. Although the maze seems real to the mouse, it is, in fact, a virtual world. Virtual reality (VR) has become a valuable tool to study brains and behaviors because researchers can precisely control sensory cues, correlating nerve-cell activity with specific actions. “It allows experiments that are not possible using real-world approaches,” neurobiologist Christopher Harvey of Harvard Medical School and colleagues wrote in 2016 in a commentary in Nature (533:324–25). Studies of navigation are perfect examples. Extraneous sounds, smells, tastes, and textures, along with internal information about balance and spatial orientation, combine with visual cues to help a mouse move through a maze. In a virtual environment, researchers can add or remove any of these sensory inputs to see how each affects nerve-cell firing and the neural patterns that underlie exploration and other behaviors. But there’s a catch. Many VR setups severely restrict how animals move, which can change nerve cells’ responses to sensory cues. As a result, some researchers have begun to build experimental setups that allow animals to move more freely in their virtual environments, while others have starting using robots to aid animals in navigation or to simulate interactions with others of their kind. Here, The Scientist explores recent efforts in both arenas, which aim to develop a more realistic sense of how the brain interprets reality. © 1986-2018 The Scientist

Keyword: Learning & Memory
Link ID: 24667 - Posted: 02.16.2018

Aimee Cunningham Knocking back an enzyme swept mouse brains clean of protein globs that are a sign of Alzheimer’s disease. Reducing the enzyme is known to keep these nerve-damaging plaques from forming. But the disappearance of existing plaques was unexpected, researchers report online February 14 in the Journal of Experimental Medicine. The brains of mice engineered to develop Alzheimer’s disease were riddled with these plaques, clumps of amyloid-beta protein fragments, by the time the animals were 10 months old. But the brains of 10-month-old Alzheimer’s mice that had a severely reduced amount of an enzyme called BACE1 were essentially clear of new and old plaques. Studies rarely demonstrate the removal of existing plaques, says neuroscientist John Cirrito of Washington University in St. Louis who was not involved in the study. “It suggests there is something special about BACE1,” he says, but exactly what that might be remains unclear. One theory to how Alzheimer’s develops is called the amyloid cascade hypothesis. Accumulation of globs of A-beta protein bits, the idea goes, drives the nerve cell loss and dementia seen in the disease, which an estimated 5.5 million Americans had in 2017. If the theory is right, then targeting the BACE1 enzyme, which cuts up another protein to make A-beta, may help patients. |© Society for Science & the Public 2000 - 2018.

Keyword: Alzheimers
Link ID: 24666 - Posted: 02.15.2018

By Andy Coghlan Surgical instruments may need to be cleaned more thoroughly after brain operations, following the news that they might be spreading proteins linked to Alzheimer’s disease. There’s no evidence yet that spreading these proteins from one person to another can cause Alzheimer’s disease itself. But a study of eight people suggests that unclean instruments may sometimes lead to a rare and potentially fatal kind of brain bleeding disorder. People who have Alzheimer’s disease typically have plaques of sticky amyloid proteins in their brains, although it remains unclear whether these are a cause or a consequence of the condition. But when amyloid builds up in blood vessels in the brain, it can sometimes make them so brittle that they leak or burst. This condition, called cerebral amyloid angiopathy (CAA), usually doesn’t develop until people reach their sixties or older. But Sebastian Brandner, at University College London, and his team have been investigating the cases of eight people who developed CAA under the age of 60. Scouring their medical records, the team found that all eight of these people had undergone brain surgery during childhood or their teenage years for a variety of reasons. Of the eight people, at least three have already died from strokes, which can be caused by CAA. They died between the ages of 37 and 57. © Copyright New Scientist Ltd.

Keyword: Alzheimers; Prions
Link ID: 24665 - Posted: 02.15.2018

By Ricki Rusting, Every morning, Avigael Wodinsky sets a timer to keep her 12-year-old son, Naftali, on track while he gets dressed for school. “Otherwise,” she says, “he’ll find 57 other things to do on the way to the bathroom.” Wodinsky says she knew something was different about Naftali from the time he was born, long before his autism diagnosis at 15 months. He lagged behind his twin sister in hitting developmental milestones, and he seemed distant. “When he was an infant and he was feeding, he wouldn’t cry if you took the bottle away from him,” she says. He often sat facing the corner, turning the pages of a picture book over and over again. Although he has above-average intelligence, he did not speak much until he was 4, and even then his speech was often ‘scripted:’ He would repeat phrases and sentences he had heard on television. Naftali’s trouble with maintaining focus became apparent in preschool—and problematic in kindergarten. He would stare out the window or wander around the classroom. “He was doing everything except what he was supposed to be doing,” Wodinsky recalls. At first, his psychiatrist credited these behaviors to his autism and recommended he drink coffee for its mild stimulant effect. The psychiatrist also suggested anxiety drugs. Neither treatment helped. A doctor then prescribed a series of drugs used for attention deficit hyperactivity disorder (ADHD), even though Naftali’s hyperactivity was still considered a part of his autism; those medications also failed or caused intolerable side effects. © 2018 Scientific American

Keyword: ADHD; Autism
Link ID: 24662 - Posted: 02.15.2018

By BENEDICT CAREY Decent memory is a matter of livelihood, of independence, most of all of identity. Human memory is the ghost in the neural machine, a widely distributed, continually changing, multidimensional conversation among cells that can reproduce both the capital of Kentucky and the emotional catacombs of that first romance. The news last week that scientists had developed a brain implant that boosts memory — an implantable “cognitive prosthetic,” in the jargon — should be astounding even to the cynical. App developers probably are already plotting yet another brain-exercise product based on the latest science. Screenwriters working on their next amnesia-assassin scripts got some real-life backup for the pitch meeting. The scientists are in discussions to commercialize the technology, and so people in the throes of serious memory loss, and their families, likely feel a sense of hope, thin though it may be. These things take time, and there are still many unknowns. But for those in the worried-well demographic — the 40-is-the-new-30 crowd, and older — reports of a memory breakthrough fall into a different category. What exactly does it mean that scientists are truly beginning to understand the biology of memory well enough to manipulate it? Which reaction is appropriate: the futurist’s, or the curmudgeon’s? The only honest answer at this stage is both. The developers of the new implant, led by scientists at the University of Pennsylvania and Thomas Jefferson University, built on decades of work decoding brain signals, using the most advanced techniques of machine learning. Their implant, in fact, constitutes an array of electrodes embedded deep in the brain that monitor electrical activity and, like a pacemaker, deliver a stimulating pulse only when needed — when the brain is lagging as it tries to store new information. © 2018 The New York Times Company

Keyword: Learning & Memory; Robotics
Link ID: 24656 - Posted: 02.13.2018

By Dina Fine Maron Suspicions of a link between prenatal ultrasound scans and autism spectrum disorder are nothing new. The technology has exploded in recent decades, giving expectant parents more detailed images of their developing offspring than ever before. And as ultrasound use has sharply increased, so too have diagnoses of autism—prompting questions about a potential relationship. A rigorous new study examining the association between ultrasounds during the first or second trimester of pregnancy and later development of autism spectrum disorder, however, delivers some good news. The study, which analyzed the medical records and ultrasound details of more than 400 kids who were born at Boston Medical Center, found there was no increase in the number of prenatal scans or duration of ultrasound exposure in children with autism compared with kids with typical development or separate developmental delays. In fact, the group with autism had less average exposure time during its first and second trimesters of development than individuals without autism did. The finding adds weight to earlier studies that suggested such scans—which use high-frequency sound waves to create an image of the fetus, placenta and surrounding maternal organs—are not a powerful enough environmental risk to cause autism on their own. But the new study, published Monday in JAMA Pediatrics, did leave one question unanswered: Does the depth of the actual ultrasound scan make a difference? The work found the children with autism were exposed to prenatal ultrasounds with greater penetration than the control group: During the first trimester, the group with autism had scans with an average depth of 12.5 centimeters compared with 11.6 centimeters for the control group. And during the second trimester the group with autism had scan depths of 12.9 centimeters compared with 12.5 centimeters for the typical development control group. Ultrasounds may not be uniform for reasons including the position of the fetus in the womb. © 2018 Scientific American

Keyword: Autism
Link ID: 24655 - Posted: 02.13.2018

By NICHOLAS BAKALAR Increasing blood sugar levels are associated with cognitive decline, a long-term study has found. Researchers assessed cognitive function in 5,189 people, average age 66, and tested their blood sugar using HbA1c, a test that accurately measures blood glucose levels over a period of weeks or months. (The finger-prick blood test, in contrast, gives a reading only at a given moment in time.) They followed the group for up to 10 years, tracking blood glucose levels and periodically testing cognitive ability. The study is in the journal Diabetologia. There was no association between blood sugar levels and cognition at the start of the study. But consistently over time, scores on the tests of memory and executive function declined as HbA1c levels increased, even in people without diabetes. The study controlled for many other variables, among them age, sex, cholesterol, B.M.I., education, marital status, depression, smoking, alcohol consumption, hypertension and cardiovascular disease. This is an observational study that does not prove cause and effect, and the lead author, Wuxiang Xie, a researcher at the Peking University Health Science Center, said that the underlying mechanism is still unknown. Still, he said, “Diabetes-related microvascular complications might be, at least in part, the reason for the subsequent cognitive decline. Future studies are warranted to reveal the precise mechanisms.” © 2018 The New York Times Company

Keyword: Learning & Memory; Alzheimers
Link ID: 24649 - Posted: 02.13.2018

Lee Burdette Williams The call came from a former colleague who coaches college students on the autism spectrum. “We’ve got someone who’s in trouble, and we could use some advice. It’s one of those Title IX things.” She told me the story. The student loves punk music and wanted to start a band. He put up fliers on the campus, which in itself was an issue because he violated the institutional posting policy. But even in today’s climate, I thought, that doesn’t usually rise to a Title IX complaint. She continued. “He wrote something in Morse code on the flyer, a message directed to women, because he was trying to recruit some to join the band. It was a little ‘stalky-creepy’ -- OK, pretty creepy -- but this guy is totally harmless and clueless and just doesn’t know how to meet women.” My first reaction was to smile. Morse code? How many college students even know what it is? But it didn’t surprise me to learn this about a student with Asperger’s syndrome, the commonly used term for those with high-functioning autism. Indeed, this kind of situation, I have come to realize, exemplifies a disastrous nexus of two trends on college campuses: the increased awareness of Title IX’s expectations for student behavior and institutional response, and the growing number of students with a diagnosis (or simply just characteristics) of autism who are attending college. I imagined the student had learned Morse code at the age of 5 and was no doubt still fluent in it. In his mind, a wondrous place created by the distinct neural connections common among those with this diagnosis, the use of Morse code to signal his interest in meeting women made perfect sense. To those who know him, it is one of many quirky characteristics -- some of them sweet, some of them annoying -- that require a bit of translation for him and about him as he moves within the world of higher education. © 2018

Keyword: Autism
Link ID: 24644 - Posted: 02.12.2018

By Roni Dengler Mental illness affects one in six U.S. adults, but scientists' sense of the underlying biology of most psychiatric disorders remains nebulous. That's frustrating for physicians treating the diseases, who must also make diagnoses based on symptoms that may only appear sporadically. No laboratory blood test or brain scan can yet distinguish whether someone has depression or bipolar disorder, for example. Now, however, a large-scale analysis of postmortem brains is revealing distinctive molecular traces in people with mental illness. This week, an international team of researchers reports that five major psychiatric disorders have patterns of gene activity that often overlap but also vary in disease-specific—and sometimes counterintuitive—ways. The findings, they say, might someday lead to diagnostic tests and novel therapies, and one has already inspired a clinical trial of a new way to treat overactive brain cells in autism. Outsiders say the data mark a milestone in psychiatry. "This [work] is changing fundamental views about the nature of psychiatric illness," says Kenneth Kendler, a psychiatric geneticist at Virginia Commonwealth University in Richmond. Researchers have long known that genes influence mental illness. Five years ago, for example, the global Psychiatric Genomics Consortium found that people with autism, schizophrenia, bipolar disorder, depression, and attention-deficit hyperactivity disorder frequently share certain DNA variations. But that 2013 study did not say how those genetic alterations might lead to symptoms. © 2018 American Association for the Advancement of Science

Keyword: Schizophrenia; Genes & Behavior
Link ID: 24638 - Posted: 02.09.2018

Laura Sanders Brain scientists have filmed a first-of-a-kind birth video. It reveals specialized cells in the brains of mice dividing to create newborn nerve cells. The images, published in the Feb. 9 Science, show intricacies of how certain parts of the adult mouse brain can churn out new nerve cells. These details may help lead to a deeper understanding of the role of this nerve cell renewal in such processes as memory. Deep in the brains of mice, a memory-related structure called the hippocampus is known to be flush with new nerve cells. But because this buried neural real estate is hard to study, the circumstances of these births weren’t clear. Using living mice, Sebastian Jessberger, a neuroscientist at the University of Zurich, and colleagues removed the outer layers of brain tissue that obscure the hippocampus. The scientists marked 63 cells called radial stem cells, which can divide to create new nerve cells. Researchers then watched these stem cells for up to two months, taking pictures every 12 or 24 hours. During that time, 42 of these stem cells underwent a spurt of division, churning out two kinds of cells: intermediate cells that would go on to produce nerve cells as well as mature nerve cells themselves. Once this burst of activity ended, the radial stem cells disappeared by dividing themselves into mature nerve cells that could no longer split. |© Society for Science & the Public 2000 - 2017.

Keyword: Neurogenesis; Development of the Brain
Link ID: 24635 - Posted: 02.09.2018